Obese Swine Research Articles

Prenatal programming in an obese swine model: sex-related effects of maternal energy restriction on morphology, metabolism and hypothalamic gene expression

Maternal energy restriction during pregnancy predisposes to metabolic alterations in the offspring. The present study was designed to evaluate phenotypic and metabolic consequences following maternal undernutrition in an obese pig model and to define the potential role of hypothalamic gene expression in programming effects. Iberian sows were fed a control or a 50 % restricted diet for the last two-thirds of gestation. Newborns were assessed for body and organ weights, hormonal and metabolic status, and hypothalamic expression of genes implicated in energy homeostasis, glucocorticoid function and methylation. Weight and adiposity were measured in adult littermates. Newborns of the restricted sows were lighter (P <0·01), but brain growth was spared. The plasma concentration of TAG was lower in the restricted newborns than in the control newborns of both the sexes (P <0·01), while the concentration of cortisol was higher in females born to the restricted sows (P <0·04), reflecting a situation of metabolic stress by nutrient insufficiency. A lower hypothalamic expression of anorexigenic peptides (LEPR and POMC, P <0·01 and P <0·04, respectively) was observed in females born to the restricted sows, but no effect was observed in the males. The expression of HSD11B1 gene was down-regulated in the restricted animals (P <0·05), suggesting an adaptive mechanism for reducing the harmful effects of elevated concentrations of cortisol. At 4 and 7 months of age, the restricted females were heavier and fatter than the controls (P< 0·01). Maternal feed restriction induces asymmetrical growth retardation and metabolic alterations in the offspring. Differences in gene expression at birth and higher growth and adiposity in adulthood suggest a female-specific programming effect for a positive energy balance, possibly due to overexposure to endogenous stress-induced glucocorticoids.

Contribution of electromechanical coupling between KV and CaV1.2 channels to coronary dysfunction in obesity

Previous investigations indicate that diminished functional expression of voltage-dependent K(+) (KV) channels impairs control of coronary blood flow in obesity/metabolic syndrome. The goal of this investigation was to test the hypothesis that KV channels are electromechanically coupled to CaV1.2 channels and that coronary microvascular dysfunction in obesity is related to subsequent increases in CaV1.2 channel activity. Initial studies revealed that inhibition of KV channels with 4-aminopyridine (4AP, 0.3mM) increased intracellular [Ca(2+)], contracted isolated coronary arterioles and decreased coronary reactive hyperemia. These effects were reversed by blockade of CaV1.2 channels. Further studies in chronically instrumented Ossabaw swine showed that inhibition of CaV1.2 channels with nifedipine (10μg/kg, iv) had no effect on coronary blood flow at rest or during exercise in lean swine. However, inhibition of CaV1.2 channels significantly increased coronary blood flow, conductance, and the balance between coronary flow and metabolism in obese swine (P<0.05). These changes were associated with a ~50% increase in inward CaV1.2 current and elevations in expression of the pore-forming subunit (α1c) of CaV1.2 channels in coronary smooth muscle cells from obese swine. Taken together, these findings indicate that electromechanical coupling between KV and CaV1.2 channels is involved in the regulation of coronary vasomotor tone and that increases in CaV1.2 channel activity contribute to coronary microvascular dysfunction in the setting of obesity.

Perivascular Adipose Tissue Potentiates Contraction of Coronary Vascular Smooth Muscle

Background— This investigation examined the mechanisms by which coronary perivascular adipose tissue (PVAT)–derived factors influence vasomotor tone and the PVAT proteome in lean versus obese swine. Methods and Results— Coronary arteries from Ossabaw swine were isolated for isometric tension studies. We found that coronary ( P =0.03) and mesenteric ( P =0.04) but not subcutaneous adipose tissue augmented coronary contractions to KCl (20 mmol/L). Inhibition of Ca V 1.2 channels with nifedipine (0.1 µmol/L) or diltiazem (10 µmol/L) abolished this effect. Coronary PVAT increased baseline tension and potentiated constriction of isolated arteries to prostaglandin F2α in proportion to the amount of PVAT present (0.1–1.0 g). These effects were elevated in tissues obtained from obese swine and were observed in intact and endothelium denuded arteries. Coronary PVAT also diminished H 2 O 2 -mediated vasodilation in lean and, to a lesser extent, in obese arteries. These effects were associated with alterations in the obese coronary PVAT proteome (detected 186 alterations) and elevated voltage-dependent increases in intracellular [Ca 2+ ] in obese smooth muscle cells. Further studies revealed that the Rho-kinase inhibitor fasudil (1 µmol/L) significantly blunted artery contractions to KCl and PVAT in lean but not obese swine. Calpastatin (10 μmol/L) also augmented contractions to levels similar to that observed in the presence of PVAT. Conclusions— Vascular effects of PVAT vary according to anatomic location and are influenced by an obese phenotype. Augmented contractile effects of obese coronary PVAT are related to alterations in the PVAT proteome (eg, calpastatin), Rho-dependent signaling, and the functional contribution of K + and Ca V 1.2 channels to smooth muscle tone.

Impaired cardiometabolic responses to glucagon-like peptide 1 in obesity and type 2 diabetes mellitus

Glucagon-like peptide 1 (GLP-1) has insulin-like effects on myocardial glucose uptake which may contribute to its beneficial effects in the setting of myocardial ischemia. Whether these effects are different in the setting of obesity or type 2 diabetes (T2DM) requires investigation. We examined the cardiometabolic actions of GLP-1 (7-36) in lean and obese/T2DM humans, and in lean and obese Ossabaw swine. GLP-1 significantly augmented myocardial glucose uptake under resting conditions in lean humans, but this effect was impaired in T2DM. This observation was confirmed and extended in swine, where GLP-1 effects to augment myocardial glucose uptake during exercise were seen in lean but not in obese swine. GLP-1 did not increase myocardial oxygen consumption or blood flow in humans or in swine. Impaired myocardial responsiveness to GLP-1 in obesity was not associated with any apparent alterations in myocardial or coronary GLP1-R expression. No evidence for GLP-1-mediated activation of cAMP/PKA or AMPK signaling in lean or obese hearts was observed. GLP-1 treatment augmented p38-MAPK activity in lean, but not obese cardiac tissue. Taken together, these data provide novel evidence indicating that the cardiometabolic effects of GLP-1 are attenuated in obesity and T2DM, via mechanisms that may involve impaired p38-MAPK signaling.

Perivascular adipose tissue impairs H2O2‐mediated vasodilation in the coronary circulation

This investigation examined the effects of perivascular adipose tissue (PVAT) on vasodilatory mechanisms in the coronary circulation. Isometric tension studies were performed on isolated coronary arteries from lean and obese Ossabaw swine. After a 30 min incubation period with 0.3 g PVAT, arteries were constricted with U46619 (1 μM) or PGF2α (10 μM) and responses to H2O2 (1 μM–1 mM) were examined. Compared to untreated‐control arteries, addition of coronary PVAT markedly attenuated relaxation to 1 mM H2O2 in lean swine (78 ± 9% vs. 17 ± 11%). This effect of PVAT was similar in intact and denuded arteries or in arteries pre‐contracted with PGF2α or U46619. However, pre‐constriction with KCl (60 mM) abolished relaxation to H2O2, implicating K+ channels in the vasodilatory response. Inhibition of K+ channels with tetraethylammonium (3 mM), penitrem A (1 μM), barium chloride (30 μM) or glibenclamide (1 μM) did not prevent relaxation to H2O2. In contrast, 4‐aminopyridine (10 mM) prevented relaxation to H2O2 to a similar degree as PVAT. Coronary arteries from obese swine demonstrated similar relaxation to H2O2, however, PVAT did not attenuate this response (98 ± 2% vs. 82 ± 8%, respectively). These findings indicate that coronary PVAT releases factors that diminish coronary vascular smooth muscle vasodilation via inhibition of K+ channels, which is absent in obesity. Support 5T32DK064466–09 and HL092245.

In vitro Release of Ovarian Progesterone is Decreased During the Oestrous Cycle and Pregnancy of Swine with Obesity/Leptin Resistance

Previous studies indicate that reproductive prolificacy of obese swine breeds is markedly influenced by embryo losses in early pregnancy. In such period, adequate secretion of progesterone (P4) by the ovary is essential for pregnancy success. This study analyses the luteal functionality during the oestrous cycle and early pregnancy of Iberian sows and Large White x Landrace females, in terms of P4 secretion after in vitro culture of luteal tissue stimulated or not with luteinizing hormone (LH). The secretion of progesterone (expressed in ng/mg of luteal tissue or ng/mgLT) of the corpora lutea of obese Iberian swine was always hampered when compared to lean genotypes, either during early oestrous cycle (110.7±37.8 vs 259.7±10.2ng/mgLT; p<0.0001), late oestrous cycle (49.0±3.5 vs 75.92±7.14ng/mgLT; p<0.0001) or early pregnancy (38.4±2.1 vs 70.7±5.3ng/mgLT; p<0.0001). The differences in basal P4 secretion remained after stimulation with LH. Finally, P4 secretion during early pregnancy of Iberian sows decreased with age and, hence, with obesity features (46.6±4.2 vs 65.5±4.8ng/mgLT; p<0.001). In conclusion, the results of the present study provide convincing evidence of a reduced luteal function during oestrous cycle and early pregnancy of sows with obesity/leptin resistance like Iberian sows, which may contribute to the low reproductive efficiency reported in this breed.

The obesity paradox and acute kidney injury: beneficial effects of hyper-inflammation?

In the general population, obesity is associated with an increased mortality risk, whereas several epidemiological studies demonstrated a protective effect of obesity in critically ill patients. In this context, Sleeman and colleagues investigated the effects of obesity on kidney function in a well-established porcine model of cardiopulmonary bypass. The authors confirm literature data that obesity per se is associated with a chronic hyper-inflammatory status. Nevertheless, obese swine undergoing the surgical procedure presented with attenuated kidney dysfunction and tissue apoptosis. The authors suggest that the chronic inflammation causes pre-conditioning against excessive acute hyper-inflammation. The authors have to be commended for using a long-term, clinically relevant model that, moreover, addresses a variety of putative mechanisms. The study is discussed in the context of the controversial findings that, in contrast to the existing literature on improved survival, most studies available suggest a higher incidence and severity of acute kidney injury in obese patients when compared with lean controls.

Testosterone attenuates metabolic syndrome and coronary artery disease in obese Ossabaw miniature swine

Epidemiological studies in humans show a strong inverse association of serum testosterone with metabolic syndrome (MetS) and coronary artery disease (CAD); however, there are no prospective experimental studies. Ossabaw miniature swine develop MetS and CAD when fed excess calorie atherogenic diet. We tested the hypothesis that castrated Ossabaws would develop greater MetS and CAD. Eight castrated and eight intact males (age 6 months) were fed atherogenic diet for 7 months. After 6 months of diet treatment we performed MetS phenotype profiling for adiposity (by computed tomography [CT]), blood pressure, glucose tolerance, total cholesterol, triglycerides, high and low density lipoprotein (HDL and LDL). Intravascular ultrasound (IVUS) imaging quantified CAD. Castrated pigs had more severe MetS than intact pigs, as evidenced by more impaired glucose tolerance, higher total plasma cholesterol, triglycerides, LDL, and LDL/HDL, and less lean mass/greater adiposity. IVUS imaging showed that castrated pigs developed more CAD, including calcification, than intact pigs. We conclude that testosterone attenuated the development of MetS and CAD in obese Ossabaw swine, thus providing an excellent model for study of testosterone therapies. (Support: Purina TestDiet, NIH HL062552)

The interaction between ovulation rate and embryo survival in determining prolificacy of different strains of obese swine with gene polymorphisms for leptin receptors

The Mediterranean Iberian pigs show a clear predisposition to obesity, due to gene polymorphisms for leptin receptors, and a lower prolificacy when compared with lean breeds. Previous studies indicate a bimodal effect of obese genotypes on prolificacy; either by lowering ovulation rate or by increasing embryo losses when compared with lean genotypes. The present study aimed to discriminate the relative influence of both parameters by comparing strains of Iberian females with different prolificacy (14 original purebred Retinto, group R, and 20 Retinto × Torbiscal females selected for prolificacy, group RT). Examination of ovaries around Day 40 of pregnancy showed a higher ovulation rate in the RT than in the R sows (21.5 ± 1.4 versus 12.3 ± 1.0 corpora lutea, respectively; P &lt; 0.0005). However, there was a higher incidence of implantation failures and early embryo losses in the RT females (42.9 versus 14% for the group R; P &lt; 0.005). Thus, the number of viable embryos was higher in the RT line (10.8 ± 0.5 versus 7.6 ± 0.7 in the R sows, P &lt; 0.0005), but also limited when compared with ovulation rate. Conversely, this effect was not found in the R sows; however, prolificacy of these females was limited by higher embryo mortality (24.1 versus 4.6% for RT females). In conclusion, the present study evidences dissimilar reproductive behaviour among strains of the Iberian pig differing in prolificacy and confirms previous evidences suggesting the existence of intrinsic factors avoiding excessively large litter sizes in Iberian females.

Overfed Ossabaw swine demonstrate resistance to the harmful cardiovascular effects of metabolic syndrome

Ossabaw swine fed a high-fat diet develop metabolic syndrome. We investigated their utility as a model for chronic myocardial ischemia in the setting of metabolic syndrome. Chronic ischemia was induced in swine fed either normal chow (lean, n=9) or a high-calorie diet (obese, n=9) by left circumflex artery ameroid placement. After 7 weeks, body weight, glucose tolerance, and serum lipids were measured. Measurements of cardiac hemodynamics, function, and perfusion were performed. Ischemic myocardium was harvested for molecular analysis. Obese swine demonstrated a 1.8-fold greater percent-increase in body weight (p=0.0003), 1.3-fold increase in mean arterial pressure (p=0.02), 5.1-fold greater fasting cholesterol (p<0.0001), and 2.1-fold greater LDL:HDL ratio (p=0.0006). Fasting glucose values were similar between groups, but glucose values after dextrose challenge were 1.3-fold greater in the obese group (p=0.04). However, myocardial perfusion, contractility, capillary density, and arteriolar density were similar between groups. Protein oxidation was reduced in the obese group, while expressions of PPAR-alpha and PPAR-gamma were 1.2-fold and 1.3 fold greater than lean animals. Thus the cardiovascular system of Ossabaw swine is protected from the deleterious effects of hypertension, dyslipidemia, and glucose intolerance, perhaps via evolutionary upregulation of antioxidant PPAR pathways.

Ovulation rate, embryo mortality and intrauterine growth retardation in obese swine with gene polymorphisms for leptin and melanocortin receptors

The Mediterranean Iberian pigs are obese genotypes, due to a leptin resistance syndrome related to leptin receptor gene polymorphisms. The Iberian pig is affected by a lower prolificacy when compared to lean breeds, and thus may constitute a good animal model for adverse effects of obesity in reproductive performance. The present study determined possible differences in rates of ovulation and embryo implantation and later incidence of embryo mortality and intrauterine growth retardation (IUGR) in sows of Iberian breed (n = 23) and highly-prolific lean commercial crosses (Large White × Landrace, n = 17) at two critical periods of swine pregnancy: Day 21 (just after achievement of trophoblast attachment) and Day 35 (just after completion of the transition from late embryo to early foetal stage). Two different reproductive performances were identified in the Iberian breed; 58.3% of the females had lower ovulation rates than LWxL (13.2 ± 2.3 vs 22.5 ± 1.6, P < 0.05), but 41.7% had a similar number of ovulations (18.2 ± 3.9). However, those Iberian sows having high ovulatory rates showed a high incidence of regression of corpora lutea and embryo losses between Days 21 and 35, which was not found in Iberian females with low ovulation rates; therefore, the number of viable embryos was similar in both Iberian groups (8.2 ± 1.0 and 8.4 ± 1.0) and lower that in highly-prolific LWxL (14.8 ± 1.8, P < 0.05). At Day 35, a total of 167 conceptuses (73 LWxL and 94 IB) were evaluated for IUGR. The LWxL conceptuses were longer and wider than Iberian (69.5 ± 0.1 and 64.4 ± 0.1 vs 49.9 ± 0.1 and 41.9 ± 0.1 mm, P < 0.0001). However, Iberian conceptuses were heavier than LWxL (107.4 ± 6.6 vs 68.6 ± 2.4 g) due to a lower quantity of fluids and a higher development of the placental tissues in comparison to the embryo itself. In conclusion, current study indicates a bimodal effect of obese genotypes on reproductive performances, either by lowering ovulation rate or by increased embryo losses in the first third of pregnancy.

Body fat content, composition and distribution in Landrace and Iberian finishing pigs givenad libitummaize- and acorn-sorghum-maize-based diets

AbstractWe aimed to determine whether the dietary carbohydrate source altered body fat composition and distribution in finishing lean (Landrace) and obese (Iberian) swine. To this end, twenty-four finishing castrated male pigs (12 Iberian and 12 Landrace; 108 kg live weight) were offered two diets differing in the main carbohydrates source, maize (diet M) or acorn-sorghum-maize (diet A). Diets were formulated to have the same nutrient content, except for carbohydrate fractions: diet M contained higher amount of starch (537v. 389 g/kg) but less non-starch polysaccharides (118v. 148 g/ kg) than diet A. At an average weight of 133 kg live weight pigs were slaughtered and their carcasses were sampled to study lipogenesis, backfat and intramuscular fat composition. Iberian pigs showed a higher voluntary food intake than Landrace pigs (3·6v. 2·4 kg/day;P&lt; 0·001) but no significant differences in the daily weight gain. Diet M tended to promote the highest food intake (P= 0·09). Iberian pigs showed higher (P&lt; 0·01) lipogenic enzyme activities, backfat thickness (71·7v. 31·9 mm) and intramuscular fat content (40 to 95 g/kg fresh muscle) than Landrace pigs, which was associated with their higher food intake. Furthermore, fat depots from Iberian pigs had higher (P&lt; 0·001) monounsaturated fatty acids (MUFA) and lower (P&lt; 0·05) polyunsaturated (PUFA) proportions than those from Landrace pigs. The backfat thickness of pigs given diet M tended to be higher (P= 0·07) than that of pigs given diet A, without differences in the intramuscular fat content. The higher backfat thickness found for diet M was correlated with a lower PUFA proportion in diet than for diet A (P&lt; 0·001). We conclude that body fat content, composition and lipogenic enzyme activities are markedly influenced by the animal breed and to a lesser extent by dietary characteristics.

The obesity gene in swine: sequence and expression of porcine leptin.

Leptin is a 16-kDa protein secreted by adipocytes that has been proposed to regulate feed intake in mice, rats, and humans. The present study was designed to characterize porcine leptin structure and expression. Successful RT-PCR resulted in development of a cDNA clone to the full length coding region of porcine leptin. Sequence data demonstrate 85% base homology to rodent, 88% to human, and a 92% homology to the bovine sequence. For assessment of porcine leptin gene expression, total RNA was extracted from the subcutaneous adipose tissue of genetically selected high backfat pigs and from contemporary crossbred swine. Total RNA derived from genetically selected high fat pigs contained 113% higher (P < .05) concentrations of porcine leptin mRNA than total RNA derived from contemporary crossbred pigs. Western blotting was used to evaluate serum levels of porcine leptin in genetically selected high backfat and contemporary, crossbred pigs. Relative levels of porcine leptin in sera from obese swine were approximately 306% higher (P < .05) than levels present in sera from contemporary, crossbred swine. These data indicate that leptin is expressed in pigs, the expressed protein is secreted into the bloodstream, and obese swine express higher levels of leptin mRNA and protein than nonobese swine at similar body weight.

Ontogeny of growth hormone (GH), insulin-like growth factors (IGF-I and IGF-II) and IGF binding protein-2 (IGFBP-2) in genetically lean and obese swine

Serum GH, IGF-I, IGF-II and IGFBP-2 concentrations were determined by radioimmunoassay in swine of genetic lines which were selected for high (obese) and low (lean) backfat. Blood samples were collected at birth, before and after nursing, at 1 and 3 days of age and at weekly or fortnightly intervals until 30 weeks of age. Overall, GH, IGF-I, IGF-II and IGFBP-2 were highest at birth and declined during the first week of postnatal life. An age-by-line interaction was apparent for GH and IGF-I during the early neonatal period with levels being higher in the lean line than the obese line at 1 day of age and similar at 1 week of age. At 3 to 5 weeks of age there was an elevation in GH which was greater in lean than obese pigs. IGFBP-2 concentration patterns were characterized by a nadir at 5 to 7 weeks of age and a decline from an apex at 8 weeks of age in both lines. IGF-II declined steadily from birth until about 10 weeks of age. A subsequent increase in IGF-II was then observed between 12 and 22 weeks, which was greater in the obese line and in male pigs but not apparent in lean females. At birth, pigs which had not nursed had higher GH and IGFBP-2 and lower IGF-I and IGF-II concentrations. The effect of nursing on IGF-I was significantly influenced by line. These data indicate that the endocrine milieu and developmental changes in the endocrine milieu of pigs with differing propensities for obesity differs, suggesting that there is an association between growth factors and physiological traits such as the development of obesity.

Ventricular energetics

Ventricular energetics

Phagocytic Functions of Pulmonary Alveolar Macrophages in Genetically Selected Lean and Obese Swine and the Effects of Exogenous Linolenic Acid upon Cell Function

Alveolar macrophages from genetically selected obese and lean swine were compared for in vitro phagocytic capabilities, using Fc(γ)- and C3-mediated phagocytosis. Cells from obese pigs were significantly more effective at Fc(γ)-mediated phagocytosis than those from lean pigs, both for percentage of total cells phagocytosing ( P<0.044) and for the average number of opsonized sheep erythrocytes (SRBC) ingested per phagocyte ( P<0.045). A seasonal interaction was noted for average number of SRBC ingested per phagocyte: the relative difference in macrophage responses between obese and lean groups became significantly more pronounced during winter and spring months ( P<0.080). Macrophages from obese pigs also exhibited higher phagocytic activities at C3-mediated phagocytosis than did cells from lean pigs, but these differences were significant only for average number of SRBC ingested per phagocyte ( P<0.080). Exogenous linolenic acid was added to selected cultures undergoing Fc(γ)-mediated phagocytosis. Addition of the fatty acid frequently caused enhanced phagocytosis. Macrophages from obese pigs were stimulated by fatty acid treatment more frequently than cells from lean pigs ( P<0.05). Relatively greater enhancement was also seen in cells from obese pigs, when compared with those from lean swine ( P<0.025). These results suggest that genetically transferred factors are of primary importance in alveolar macrophage phagocytic responses and that linolenic acid can induce increased phagocytic activity by porcine alveolar macrophages in vitro.

Comparative Response of Lean or Genetically Obese Swine and Their Progeny to Severe Feed Restriction During Gestation

Genetically obese (O) or lean (L) primiparous gilts were assigned on the day of mating to an adequate [control (C) or restricted (R)] intake of feed. Body weight and ultrasonically estimated backfat depth were recorded at wk 0 (mating), 4, 8, 12 and 16 of pregnancy, and at d 2-3, 21 and 28 of lactation. Number of pigs born, survival rate to 28 d of age and piglet body weight at 0, 14, 21 and 28 d of age were recorded. Four male and four female progeny from each diet group of each genetic strain were slaughtered at 6 mo of age for carcass and organ weight measurements. OR and LR gilts responded similarly to feed restriction in body weight change, backfat depth and plasma traits. Body weight increased throughout gestation in OC and LC gilts but decreased about 6 kg in OR and LR gilts. Backfat remained relatively constant throughout gestation in OC and LC gilts but declined steadily in LR and OR gilts. There were no genetic group x diet interactions for any trait measured. Litter size and piglet survival were not affected by diet or genetic group, but piglet birth weight and daily gain to d 28 and to wk 25 were lower in both R groups. Backfat accretion and other indices of carcass fatness were reduced in progeny of R dams.(ABSTRACT TRUNCATED AT 250 WORDS)

(3) Pulmonary alveolar macrophage responses of genetically selected obese and lean swine during acute Toxoplasma gondii infections

(3) Pulmonary alveolar macrophage responses of genetically selected obese and lean swine during acute Toxoplasma gondii infections

Sera-controlled preadipocyte growth in culture: an ontogeny study with sera from lean and obese pigs.

Genetically lean and obese swine were used to investigate the control of preadipocyte growth in culture by porcine serum. Sera were collected from fetuses from obese and lean strains at 70, 90 and 110 d of gestation. Postnatal serum samples were collected from both lines of pigs at 23 to 27 kg. Rat preadipocytes were isolated and grown in culture. Preadipocyte and stromal-vascular cell proliferation was greater in cultures grown in sera obtained postnatally than in cultures grown in sera from fetuses. Sera from lean and obese fetuses were equipotent in promoting cell proliferation. Glycerol-phosphate dehydrogenase (GPDH) activity was higher in cultures fed serum from obese pigs and fetuses than in cultures fed serum from lean pigs and fetuses. Cultures grown in serum from obese fetuses and pigs had soluble protein levels similar to cultures grown with serum from lean pigs and fetuses. These results demonstrate that serum from genetically obese swine, in the pre-obese (fetal) and obese (postnatal) state, caused increased adipogenic activity in adipocytes in culture.

Blood parameters and body composition in fetuses from reciprocal crosses of genetically lean and obese swine.

Lines of swine previously selected for either high backfat (obese) or low backfat (lean) were investigated to determine the effect of maternal obesity and the relationship between serum parameters and body composition. Fetal weight, percentage body protein, fat, fat-free organic matter and ash, and serum concentrations of albumin, growth hormone, triiodothyronine, and cortisol were compared in fetuses from straight line and reciprocal crosses at 110 days of gestation. Fetuses from the obese line weighed less but had a greater percentage body protein, fat, and fat-free organic matter than did fetuses from the lean line. Serum concentrations of albumin and triiodothyronine were less whereas those of growth hormone were greater in fetuses from the lean line compared to fetuses from the obese line. Values for these parameters in fetuses from the reciprocal crosses were generally intermediate to those of fetuses from the lean and obese lines. Comparisons of fetuses from the reciprocal and line crosses by linear contrast showed that the observed differences were mainly due to the average genetic effect of individual fetal genotypes and not due to maternal effects. Correlations computed from the residual variance showed a positive relationship between percentage body protein, serum albumin, and triiodothyronine while percentage body fat was not correlated with any of the other traits. Serum growth hormone was negatively correlated with fetal weight. We conclude that there is no apparent maternal effect of obesity or relationship of fetal fat content with any of the other variables measured in these lines of swine at the stage of fetal development at which these determinations were made.